Endod Dent Traumatol 2000; 16: 240250 Printed in Denmark .

All rights reserved

Copyright C Munksgaard 2000

Endodontics & Dental Traumatology

ISSN 0109-2502

Review article

Pulp capping with adhesive resin-based composite vs. calcium hydroxide: a review
Schuurs AHB, Gruythuysen RJM, Wesselink PR. Pulp capping with adhesive resin-based composite vs. calcium hydroxide: a review. Endod Dent Traumatol 2000; 16: 240250. C Munksgaard, 2000. Abstract The results of some short-term experiments suggest that direct capping of a vital pulp with the modern resin-based composite systems may be as effective as capping with calcium hydroxide. Total cavity etching with 10% phosphoric acid seems to be safe for the exposed pulp, but unless annulled by calcium hydroxide 35% phosphoric acid may be disastrous. For hemostasis and cleaning of the pulp wound both sodium hypochlorite and saline seem suitable, whereas the effectiveness of a 2% chlorhexidine solution is questionable. Although hard-setting calcium hydroxide cements may induce the formation of dentin bridges, they appear not to provide an effective long-term seal against bacterial factors. Within a few years, the majority of mechanically exposed and capped pulps show infection and necrosis due to microleakage of such capping materials and tunnel defects in the dentin bridges. It is unknown whether newer types of resin containing calcium-hydroxide-products will act as a permanent barrier. The cytotoxicity of the resin-based composites and the temperature rise during polymerisation may not be of concern, but microleakage, sensitisation and allergic reactions may pose problems. Based on available data, pulp capping with resin-based composites may be said to be promising, but more and long-term research is mandatory before the method can be recommended.
A. H. B. Schuurs, R. J. M. Gruythuysen, P. R. Wesselink
Department of Cariology, Endodontology and Pedodontology (CEP), Academic Centre for Dentistry Amsterdam (ACTA), Amsterdam, The Netherlands

Key words: calcium hydroxide; microleakage; pulp capping; resin composite A. H. B. Schuurs, CEP, ACTA, Louwesweg 1, 1066 EA, Amsterdam, The Netherlands Accepted June 27, 2000

The exposed vital pulp possesses a potential to heal. Direct pulp capping is a procedure in which an exposed pulp is covered with a dressing or cement that is placed directly at the site of the exposure, by which the pulp is protected from additional injury, permitting healing and repair. None of the pulpal tissue is removed. Even after 24-hour exposure to the oral environment the supercially infected pulp may show repair by the formation of dentinal bridge (1, 2). Infection, necrosis of the pulp, internal resorption and 240

obliteration of the root canal(s) indicate failure of the treatment. The formation of a dentin bridge implies that the pulp has survived at least temporarily, but it may still become necrotic. A dentin bridge may be viewed to represent wound healing, but it may also signify irritation. On the other hand, the formation of a bridge is not a requirement for a successful treatment outcome (3). Traditionally, mechanically exposed, but otherwise healthy pulps of permanent teeth have been capped

Pulp capping with composite vs. calcium hydroxide

with a wound dressing of calcium hydroxide (Ca(OH)2). A disadvantage of this material is its tendency to dissolve within 12 years, which may sometimes be observed clinically (see paragraph 2). The direct contact of the pulp with other materials, like composite resin or silver amalgam, does not permanently irritate healthy pulps, provided that bacterial leakage is prevented (47). Therefore, capping the exposed, vital pulp with adhesive resin-based composites systems (ACSs) has been suggested. This may possibly provide a longer lasting bacterial barrier than Ca(OH)2. Capping with ACSs has been studied experimentally over the past few years. Both Ca(OH)2 and ACSs have their proponents and adversaries. The present article is a literature-based assessment of whether pulp capping with ACSs is justied.
Pulp capping with calcium hydroxide

One of the essentials in capping the exposed healthy, or supercially infected (8), pulp is control of bleeding during the capping procedure. A blood clot prevents the close contact between the capping material and the pulp and may serve as a potential substrate for bacterial growth, resulting in chronic inammation with internal resorption (3) or necrosis of the pulp. Control of pulpal bleeding with simple means seems a clinically reliable method to asses whether the pulp is hyperaemic and inamed and whether pulp capping is indicated. In case, in spite of several attempts, the bleeding fails to stop, indicating inammation, other treatment modalities should be considered. The prevention of bacterial activities by the capping material seems also essential. First, it may kill some microorganisms that contaminate the wound surface and, second, it may protect against microbial effects of microleakage. For this purpose Ca(OH)2 is often used. However, pure Ca(OH)2 hydroxide and various hard-setting Ca(OH)2-containing cements, such as LifeA (Kerr, Romulus, MI, USA) and DycalA (Dentoply Caulk, Milford, DE, USA), may not so much prevent microleakage, but suppress infection by a bactericidal action due to the release of hydroxyl ions. The caustic effect of Ca(OH)2 does not seem to impart permanent damage to the pulp (9), and a slightly toxic or irritative effect may be needed to promote the cellular reorganisation of the pulp and the reparation of the exposure with dentin formation. The supercial layer of the pulpal tissue necrotizes subjacent to Ca(OH)2. The formation of this necrotic layer is considered of importance for stimulation of the nearby healthy pulp cells to transform to odontoblast-like cells, which in turn attempt to bridge the exposure with new dentin. After pulpotomies three separate necrotic zones are distinguished; a mummied supercial layer, an intermediate layer, in which the hydroxyl ions are neutralised, and an apical layer

(2). Inammatory cells migrate into the apical layer and macrophages remove the necrotic tissue debris. Fibroblasts and endothelial cells originating from the central pulp become arranged along the necrotic zone. The shape of the broblasts changes to cuboidal (odontoblast-like), which would, however, not be required in small pulp exposures. The broblasts synthesise a brodentinal matrix, which becomes calcied with minerals delivered by the blood supply and probably the dressing material. Fibronectin, which binds TGF-b, is considered to induce cytological and functional differentiation of odontoblast-like cells (11). It has been debated whether healing of the exposure is specic for Ca(OH)2 (2, 7, 10, 11). Ca(OH)2 dressings of hard-setting Life and Dycal dissolve clinically within 12 years. Since the majority of dentin bridges under the capping appear to contain tunnels, some 50% of the pulps may show infection or become necrotic due to microleakage (12). Ca(OH)2 has other disadvantages as well. Both a suspension of pure Ca(OH)2 and the hard-setting liners such as Life and Dycal, are degraded by etching and rinsing prior to restoration with ACS (13). Ca(OH)2 itself does not adhere to the dentin (14). In newer products (Advance Formula DycalA, Prisma VLC DycalA) the Ca(OH)2 is incorporated in urethane dimethacrylate with initiators and accelerators (15), by which they bind to the dentin and have a higher resistance to acid dissolution (9). They are, however, not insoluble as they still allow (9) the desired release of OH and are found in macrophages (2, 10). The urethane dimethacrylate in the newer Ca(OH)2 formulas may to be safe to the pulp (15), but Ca(OH)2 itself inhibits the polymerisation of adhesive resins (13). Cement bases of Dycal and Life cannot withstand the condensation of amalgam in spite of their early compressive strength (14). The newer Ca(OH)2-containing products are reported to be stronger and seem to be compatible with ACSs, that is to say, have been used in combination with ACSs (9).
Alternatives

The disappointing results of Ca(OH)2 have prompted the search for other capping materials. The suspension of pure Ca(OH)2 and the older hard-setting liners may be covered with a variety of base materials. One of these is ZnO-eugenol cement (8), which sealing ability may be based rather on its bactericidal properties (16), i.e. a biological seal, than prevention of microleakage, e.g. a mechanical seal (17). However, the degree of inammation after pulpotomies suggests the eugenol released (by IRMA, L.D. Caulk, Milford, DE, USA) to be more damaging to the pulp than polycarboxylate cement and formocresol (18). Placed directly on the pulp, ZnO-eugenol resulted in inammation and necrosis (19). It is not unlikely that 241

Schuurs et al.

the eugenol leaching from the cement diffuses through the Ca(OH)2 suspension and liners. On the other hand, based upon tests with three-dimensional cell cultures and good compatibility with the dental pulp when placed on intact dentin, the toxicity of zinc oxide and eugenol is questionable (20). A disadvantage of ZnO-eugenol cement is its incompatibility with the ACSs. Alternatively, Ca(OH)2 may be covered with a polyacid modied resin-based composite (compomer) or a resin-modied glass ionomer cement, which seal better than glass ionomer cement (21, 22), but further study in regard to microleakage seems needed (23). In deciduous teeth short-term results of pulpotomies with resin-modied glass ionomer cements as a sealing over Ca(OH)2 are promising (24). Compomers appear to be free of gaps after six months (25), but long-term studies are lacking. In the absence of bacteria the compomers are found to be biologically compatible with non-exposed pulps (26). Unpublished retrospective data on deciduous teeth in our clinic seem to support this observation. Both compomers and resin-modied glass ionomer cements are compatible with ACSs. However, by using Ca(OH)2 with such cements and composite (or amalgam), the total restoration consists of three materials, which may complicate the technical procedures. The modied cements themselves could possibly, without Ca(OH)2, serve to cap the exposed vital pulp. It is insufciently known which components leach from these cements (27). The cements contain monomers, which if leached out in sufcient large quantities may be toxic to the pulp. Their photosensitisers, such as camphorquinone and 9-uorenone, may have a cell-damaging effect, by their ability to generate reactive oxygen (28). However, both compomers and resin-modied glass ionomer cements are found to leach mainly HEMA (2-hydroxyethylmethacrylate) (and uoride), in particular during the rst hours after setting (29). The release of large quantities of HEMA, greater when they are incompletely cured (30), may explain why the resin-modied glass ionomer liner VitrebondA (3M, St. Paul, MN, USA) appears to be toxic in cell cultures (31) and more bactericidal than Ca(OH)2 (32). Due to or in spite of these features, experimental partial pulpotomies with VitrebondA without Ca(OH)2 were as successful as with Ca(OH)2 (33). The resin-modied glass ionomer cement VitremerA (3M, St. Paul, MN, USA) was found to be signicantly more toxic than Fuji II LCA (GC, Tokyo, Japan), but still could be classied as slightly toxic (34). In any case, capping and lling with one and the same material is less complicated, but the long-term efcacy and safety of resin-type glass ionomer cements and compomers as capping material need still to be demonstrated. Furthermore, they cannot serve as permanent occlusal llings. 242

Composite systems: specic factors

ACSs may allow to cap and ll with one permanent material. Capping with ACSs is only acceptable if the results are at least equal to those with Ca(OH)2. The ACSs may be harmful to the pulp by the etching acid, toxicity of the leached components, microleakage due to polymerisation shrinkage and demineralised dentin incompletely penetrated by the bonding (nanoleakage), sensitisation, and temperature rise during setting. The separate effects of these factors are difcult, if not impossible, to assess and synergistic effects may occur. Yet, an attempt will be made to discuss each of these factors.
Effect of acid

Acid and unexposed pulp Acid etching of the dentin is nowadays a generally accepted procedure. The acids apparently do not or only temporarily harm the pulp (35, 36) as long as 1 mm dentin remains so that the concentration of the diffusing acid is substantially diminished (37). Even phosphoric acid with pH 3.5 applied on 0.5 mm remaining dentin does not cause more frequently pulp inammations than distilled water (38). The reduction in concentration of the diffusing acid is the consequence of interactions with the hydroxylapatite and the proteins in the tubules. It seems like it is not the acid, but microleakage, which causes harm (39). The question whether a direct contact of the etching acid with the exposed pulp is safe, has not been answered, but from the data of capping with acidic cements some conclusions may be drawn. Acidic cements on exposed pulp The acidic phosphate cements (pH1.5) become neutral only days after mixing. Direct capping with phosphate cements and silicate cements induce pulp reactions, which disappear within 21 days, on the condition that microleakage is prevented with a cavosurface seal of ZnO-eugenol cement (40). Without such a seal, the reactions persist and no dentin bridge is formed (40). The amount of the released, unreacted phosphoric acid of the cement may however be relatively small compared to the amount of free acid used to etch prior to capping with an adhesive composite system (ACS). Etching acids directly applied to the pulp To our knowledge, only one study suggests that acid etching is damaging to the exposed pulp. Other studies do not show such negative results. These studies are described briey. Cavities with mechanically exposed pulps were contaminated by 60 s contact with saliva. Hemostasis was controlled with a disinfectant (ConsepsisA, a 2%

Pulp capping with composite vs. calcium hydroxide

chlorhexidine solution; Ultradent, South Jordan, UT, USA). The cavities were etched with 35% phosphoric acid, and the pulps were capped and the cavities lled with various ACSs. Etching after application of Consepsis resulted in renewed pulpal bleeding, which was difcult to control. From day 5 to day 75 an increasing number of pulps became necrotic although only very few microorganisms could be detected histologically. In most teeth dentin bridges were absent, in spite of attempts to form a bridge. When, however, after application of Consepsis and etching the pulp was capped with Ca(OH)2 (Dycal or Ultrablend VLCA; Ultradent, South Jordan, UT, USA), followed by a second etch and restoration with ACSs, fewer pulps narcotised and in many instances bridges were formed (9). These data suggest that Ca(OH)2 diminishes the pulpal damage of either the acid or Consepsis. Even more pulps survived if Ca(OH)2 was applied after use of Consepsis, but prior to etching (9). Cavity etching for ACS restoration with 35% phosphoric acid was concluded to be diastrous for the exposed pulp (9). As can be seen in Table 1, this acid seems damaging indeed, unless annulled by Ca(OH)2. It has been suggested that it may not be 35% phosphoric acid, but Consepsis which was toxic to the pulp (10). Consepsis is a good to excellent hemostatic agent (9), but the subsequent etching with 35% phosphoric acid caused renewed pulpal haemorrhage that was difcult to control with a second application of Consepsis (9). If Consepsis, or the bleeding, caused failure of pulp capping with ACSs the results of Consepsis with Ca(OH)2 capping (and ACS restoration with ACSs) should also have been bad, but the latter was not the case, as may be seen in Table 1. Therefore, 35% phosphoric acid seems disastrous indeed to the vital pulp, although dentin chips in the supercial pulp tissue may reduce the destructive action of the acid (9). Etching acids other than 35% phosphoric acid and hemostatic agents other than Consepsis are available. Promising results are obtained in other studies with ACSs. Etching of exposed pulps after provisional capping with Ca(OH)2, thereafter replaced by a glutaraldehyde-containing adhesive and composite, does not result in clinically or radiographically observable adverse pulpal reactions within 26 months (41). Pulp capping with the use of 2.5% sodium hypochlorite for
Table 1. Simplied study design and results of Pameijer & Stanley (1998) (9) Materials used Group 1. 2. 3.
a

control of bleeding, followed by etching with several kinds of acids of various concentrations (Table 2), and capping/restoration with different ACSs appears to match the performance of Ca(OH)2 (Table 3), but some brands of ACSs (notes Table 2) perform poorly. Although the evaluation periods in most of these studies are restricted to months, it seems unlikely that a detrimental effect of the etching acid would appear at later time periods. Conclusion Etching acids seem not to harm the exposed pulp permanently, with the possible exception of 35% phosphoric acid, unless in the latter case Ca(OH)2 is applied as well. Hemostasis with sodium hypochlorite or a saline solution may be more effective and safer than a 2% chlorhexidine solution (Consepsis).
Toxicity of composite systems as direct capping agents

All the organic components of the ACSs (27), the photo-inititators (48, 49), the ller and its elements (50) as well as constituents generated during the setting process (51), are released, in particular shortly after setting (48). In eluates, the amounts released vary from brand to brand (27, 48, 51, 52, 53). The higher the degree of chemical conversion, the lower the release of leachables (53). The base monomers, consisting of larger molecules of Bis-GMA (2,2-bis[4(2-hydroxy-3-methacryloxypropoxy) phenyl] propane) and UDMA (urethane dimethacrylate), may not be released (49), or just in very small quantities, possibly because their solubility in water is low (more in saliva, and thus likely in pulp uids too) (27, 52). In contrast with the smaller, additive monomers such as HEMA and TEGDMA (triethyleneglycol dimethacrylate), the base monomers may not readily diffuse through the body of the lling. But when (thick) layers of composite are insufciently photocured, the conversion into polymer may be very incomplete (54), and this will promote the release of several monomers. Also the colour of the ACS and size of the ller may inuence the curing depth negatively (55). Moreover, after setting, hydrolytic degradation of the adhesive (56, 57) and deterioriation of the adhesive and composite due to enzymes (esterase, lipase) may occur (58, 59). The deterioriation products might be cytotoxic. Cell cultures The monomers, among which the relatively small molecules of TEGDMA and HEMA, are found to be cytotoxic in cell cultures and to affect the metabolism of the cells (6065). Synergistic (additive) effects of the separate constituents of ACSs on the cells are rarely studied, but most probably exist (66). In cell cultures the monomers appeared to be less 243

Consepsis yes yes yes

b

Acid on npulp yes yes no

Capped with: bonding Ca(OH)2 Ca(OH)2

Etching of Ca(OH)2 yesa nob

Bridges 25% 71% 82%

50% of the cases.

In one subsample the enamel was etched.

Schuurs et al.
Table 2. Results of pulp capping with adhesive resin-based composite systems. The materials used are presented in the order of application. Findings after weeks and months are taken together (Inam.inamed pulp; Necrot.necrotic pulp; Attemptattempt to form a dentin bridge; incomplete bridge; Yescomplete bridge) % pulps Materials (Authors) Consepsis 35% H3PO4 bonding (Pameijer & Stanley, 1998) (9) NaOCl 10% H3PO4 bonding (Otsuki et al., 1997) (42) NaOCl 10% maleic acid bonding (Tsuneda et al., 1995) (43) Saline solution 10% maleic acid bondingb (Pereira et al., 1997) (44) NaOCl bonding 37% (?) H3PO4C (Tsuneda et al., 1995) (43) NaOCl bonding 10% citric acid (Tsuneda et al., 1995) (43) Lidocaine/epinephrine H2O2/NaOCL 10% citric acid bonding (Kitasako et al., 1999) (45) Lidocaine/epinephrine H2O2/NaOCL 10% citric acid/3% ferric chloride bonding (Kitasako et al., 1999) (45) Lidocaine/epinephrine H2O2/NaOCL bonding (Kitasako et al., 1999) (45) ? Bonding (Katoh, 1994) (46) NaOCl bondingsf (Cox et al., 1998) (10) (Akimoto et al., 1998) (47) Saline solution bondings ( 37% H3PO4 on enamel)f (lmez et al., 1998) (13)
a e

% with bridges Attempt Yes

Inam.

Necrot.

40 28 10 30 10 20 20 20 20 21 91 25 24

? 18 100A 100 0 ?d 15 80 20 14 15 20 33

45 ? 100 0 100 0 0 0 0 0 9 0 0

40 64 0 ? ? 70 5 5 10 ? ? 92

75 90 65 95

8 0 0 0 20 5 25 87 88

After 30 days, necrotic within 90 days. Scotchbond MultiPurpose with Z100A (3M, St. Paul, MN, USA). c Tokuso Light Bond and One allA (Tokuyama, Yamaguchi, Japan) (identical to Scotchbond MultiPurpose with Z100). d With Superbond C&B (Sun Medical, Kyoto, Japan) and Clearll Liner Bond (Kuraray, Osaka, Japan) the majority of the inamed pulps recovered slowly. e Superbond C & B (brush-on technique). f Different composite systems.
b

toxic in the presence of dentin (67, 68), but the smaller monomer molecules, such as HEMA and TEGDMA diffuse through the dentin, even against an externally oriented uid ow (63, 69). A decrease in the thickness of the remaining dentin results in more diffusion (70). After polymerisation of ve adhesives, in particular one (Solobond Plus, VOCO, USA) released a relatively large amount of TEGDMA in de-ionized water. Of the eluted chemical compounds, TEGDMA is reported to be the most cytotoxic. TEGDMA almost completely inhibits proliferation of cultured broblasts (71). Others found in terms of TC50 values the rank order: Bis-GMAUDMATEGDMAHEMA (62). Applied against the pulp, the dentin barrier is absent. The pulp is a more complex environment than a cell culture and the concentrations of the ACSs components will decrease by dilution and transport. Removal of UDMA and Bis-GMA from cell cultures allowed the recovery of the cultures unless the concentrations were 244

high (72, 73). Thus, healing of pulpal damage, if any, by toxic products, may be possible. The question arises whether ACSs in direct contact with the pulp release sufciently large amounts of components to be cytotoxic, i.e. cause a non-bacterial pulpal inammation or necrosis. A supercial necrosis of the pulp in the absence of microbes does not necessarily mean a negative prognosis. Pulp Microleakage of bacteria and their products cause pulp reactions, which will persist due to their continuing supply and which may nally end with necrosis. If on the other hand toxicity of the constituting components of the ACSs, e.g. (non-reacted) monomers, induce the pulp reactions, the observed decrease in the release of the components may account for a reduction and disappearance of the reactions (63). Some experiments give information on the toxicity

Pulp capping with composite vs. calcium hydroxide

Table 3. Results of pulp capping with Ca(OH)2. The materials used are presented in the order of application. Findings after weeks and months are taken together (Inam.inamed pulp; Necrot.necrotic pulp; Attemptattempt to form a dentin bridge; incomplete bridge; Yescomplete bridge) % pulps Materials (Authors) Consepsis Ca(OH)2 (Pameijer & Stanley, 1998) (9) Consepsis 35% H3PO4 Ca(OH)2 bonding (Pameijer & Stanley, 1998) (9) NaOCl Ca(OH)2 bondingsa (Cox et al., 1998) (10) NaOCl Ca(OH)2 amalgam (Akimoto et al., 1998) (47) Ca(OH)2 37% H3PO4 bonding (Heitman & Unterbrink, 1995) (41) Saline solution Ca(OH)2 10% maleic acid bonding (Pereira et al., 1997) (44) Lidocaine/epinephrine H2O2/NaOCL Ca(OH)2 bonding (Kitasako et al., 1999) (45) Saline solution Ca(OH)2 amalgam (lmez et al., 1998) (13)
a

% with bridges Attempt Yes

Inam.

Necrot.

28 28 30 20 8 30 20 12

? ? 20 35 0 ? 35 67

11 22 0 0 0 ? 0 17

7 7 ? ? ? 0

100 63 67

83 72 93 93 ? 37

Different composite systems.

of ACSs in direct contact with the pulp. When microleakage does not occur, histologically no pulpal harm is observed (6). Capping with ACSs resulted in the formation of (in)complete dentin bridges in 85% of the cases within 16 months, in spite of some microleakage (46). Nevertheless, with Permagen (Ultradent, South Jordan, UT, USA) more pulps became necrotic than with other bondings (9), but it is not clear whether toxicity is responsible. Capping and lling (brush-on technique) with Superbond C & B resulted in the development of an inammatory cell inltration in the pulp, while histologically no bacterial penetration along the cavity walls could be detected, but ndings with other bondings were much better (45). According to other studies, the results of pulp capping with various ACSs are almost equal to those with Ca(OH)2; three months after capping the frequencies of damaged pulps are similar, the reactions do not differ in severity, and approximately the same percentages of teeth show bridges (10, 13, 47). Capping with an ACS after hemostasis with HemodentA (Premier, Norristown, PA, USA) and total cavity etching with 10% phosphoric acid resulted in bridge formation in asymptomatic pulps (74). However, the ndings of subacute foreign body response in the pulp around composite particles and of persistent chronic pulpitis without bridge formation call for further studies (74). Lastly, other effects of bonding components, such as 2-hydroxyethyl methacrylate, must be studied. For instance, if present in sufciently high concentrations, the components may suppress the secretion of inammatory mediators from macrophages (75), but the clinical implications are unknown.

Estrogenicity Dental sealants, based upon Bis-GMA, would release bisphenol-A and bisphenol-A dimethacrylate in the mouth. Just like estradiol these ingredients were found in vitro to stimulate proliferation of breast cancer cells (76). The release of such estrogenic ingredients from sealants could, however, not be conrmed (77). The incomplete conversion of the monomers of composite resins or impurities from their production (78), may be sources of small quantities of an unknown component resembling bisphenol-A and bisphenoldimethacrylate, a possible estrogenic drug, which have been found in eluates of set sealants (79). Eluates of set composites contained all monomers, including bisphenoldiacrylate (53). In a recent, critical review it was concluded that the amounts of these (not very potent) estrogenics released are too small to affect the reproductive tract, but that under extreme conditions the release of estrogenic impurities in Bis-GMA-based resins could induce a weak estrogenic effect on target tissues. The short-term risk of an estrogenic effect was concluded to be insignicant, but the long-term risks were assessed to need further study (78). The American Dental Association states that there is no evidence of an estrogenic action of Bis-GMA and its components, but advises monitoring for adverse effects, as must be done for all restorative materials (80). The above mentioned conclusions relate to the use of Bis-GMA products in the mouth. The direct application of Bis-GMA-based resins on connective tissues, c.q. the pulp, implies a different route of administration and demands therefore extra monitoring. 245

Schuurs et al.

Conclusion Toxic effects of ACSs on the pulp are in general either absent or transient, but one cannot exclude that some brands may be toxic. Estrogenic effects of the ACSs directly placed on the pulp need to be studied, just as pulp reactions to tissue-embedded composite resin particles.
Bacteria

Microleakage The monomer molecules become packed closer during polymerisation of the ACSs, leading to bulk contraction. Maximum conversion into polymer improves the physical properties of the ACSs and may diminish the leaching out of components. However, extensive conversion may promote polymerisation shrinkage of the ACSs, which may result in more leakage and thus bacterial penetration. The ACSs have little if any bactericidal properties (81). However, a disinfecting activity of the self-etching primers, which are not rinsed away with water, eliminates more or less the bacteria remaining in the demineralised smear layer (82). The question remains whether etching acids create a situation free of bacteria (83). But even if bacteria are eliminated during restoration, microleakage from the nished restoration must be controlled. Many studies have reported on gaps and microleakage. Even with the newest generations of adhesives (8487), the bonding to the enamel and dentin is not always complete. Differences exist by brand and viscosity of the bonding (88, 89). Incomplete bonding results in gaps along the cavity walls (56, 9092), caused by partial disruption of the adhesive bond (93) without a decrease in bond strength (94, 95). Microleakage is said to be substantial (17), especially along the cement/dentin walls and along dentin with few tubuli (90). Microscopic gaps, which do not allow bacterial ingress, may still allow the diffusion of bacterial toxins (96). If the bonding does not inltrate the total width of the demineralised dentin (84, 97, 98), bacteria or their toxins may invade the collagen layer (nanoleakage) (99). This was the reason for recommendations to use lower concentrations of the acid in order to facilitate the primer and the bonding agent to penetrate the total width of the smaller, demineralised layer consisting of the collagen bril network (97). Overetching with 35% phosphoric acid did not affect the bond strength in the short-term, but it increased nanoleakage, which raises concern about the long-term stability of the hybrid resin-dentin layer (100). Other factors have also a negative inuence on the quality of the hybrid layer; e.g. insufcient drying or photocuring of the primer of All Bond 2 (Bisco, Schaumburg, IL, USA) furthered microleakage, but even after cor246

rect application some microleakage still was present (101). In spite of absence of a hybrid layer (102), the microleakage of Prisma Universal Bond 3 (L.D. Caulk, Milford, DE, USA) was small compared to that of Gluma (Bater AG, Leverkusen, Germany, whereas Clearl PhotoBond (Kuraray, Osaka, Japan) performed the best (103). Of the multitude of studies performed, only a few indicate that composite restorations are free of gaps along the cavity walls. Photopolymerisation initially at low and next at high light-intensity reduces the polymerisation stress (104), and may help to prevent gap formation (105, 106). The restoration technique inuences the microleakage. Resin restorations placed in bulk will show more gaps than restorations placed in two layers (85) or more (92). But some studies indicate that bulk-lling generates comparatively less stress from polymerisation shrinkage than incremental lling techniques (107, 108). Sufce it here to say that the clinical perfection needed to make an adequate composite restoration is not guaranteed in every clinical situation (20). In order to serve as a capping material, ACSs may show microleakage neither on the short-term nor in the long run. The wall adaptation of the ACSs has been reported to decrease brand-dependent with time (88, 109). The bond strength of some adhesive systems may increase by thermocycling (111), but at the same time the microleakage, which is (partly) independent from the bond strength, increases (111). Short-term microleakage may be absent or limited at least for months; bacterial toxins therefore may not reach the pulp. Within six months, however, the microleakage along the dentinal walls increased for some brands of ACSs, but not for others (25). Moreover, the bond strength to the dentin appeared to deteriorate with time (112, 113); after three years the bond strength had decreased by about 50% (114). Although bond strength and microleakage are not identical, one may expect them to inuence each other. The long-term stability of the resin-dentin attachment remains to be evaluated (90).
Microleakage and vital pulp capping

After restoring cavities without pulp exposition with Clearl, which shows a relatively large polymerisation shrinkage, bacteria were seen in the dentin of teeth with pulp inammation, while this was not the case after restoration with Ca(OH)2 and amalgam (47). It is not expected that in case of an exposed pulp the ndings will be better. In one recent study, two thirds of the teeth with necrotic pulps capped with ACSs showed bacteria histologically, sometimes at great distance from the exposure site; their numbers were, however, small (9). Remarkably, the absence of bridges correlated only

Pulp capping with composite vs. calcium hydroxide

moderately with the presence of microorganisms (9). It should be noted that in order to see organisms in microscopic slides, many must be present (115). Another histopatholigical study showed severe pulp responses in association with microleakage after pulp capping with two of the four ACSs studied. Capping with two non-leaking composites often resulted in bridge formation within the three months observation period, but not under two ACSs showing microleakage (43). When combined, in another study with a CA(OH)2 capping material one, of the two failing composite systems showed formation of dentin (44). In one study, fewer bacteria were found along and underneath restorations when capped with CA(OH)2 compared with different ACSs (10), but in this regard the ndings of others are contradictory (13, 47). Conclusion Microleakage is assessed to be important to the health of the exposed pulp. It appears that the degree of microleakage is determined to a large extent by the brand of the composite system (116), and most probably as well by the skills of the operator. A few of the ACSs show pulp-damaging microleakage within a short time period. Microleakage of the other ACSs on the long-term needs study.
Allergy

such Type I reactions, but to our knowledge, this has been reported neither in clinical case reports nor in experimental studies.
Temperature

Photocuring causes a small increase in the local temperature, which increases the degree of conversion of the monomers (94). The temperature rise of a composite lling and its environment during photocuring for 40 s is at the average 5.4 C with a maximum of 11.7 C (125). In primates an intra-pulpal temperature rise of about 5 C irreversibly damages 15% of the pulps, and a rise of 12 C, 60% of the pulps (126). However, in human volunteers a mean pulpal temperature rise of 11 C (8.9 14.7 C) maintained for 13 min is needed to cause pain. In the months thereafter pain and histological alterations of the pulp are absent (127). Based upon experiments in humans (125, 127), permanent damage by the curing temperature is questionable. However, in case of pulp capping with ACSs an isolating layer of dentin is absent. Clinical studies and case reports regarding pulpal heat damage by photopolymerisation of ACSs during capping are lacking, which may be a positive sign. Conclusion In clinical trials of pulp capping with ACSs thermal damage is not mentioned and seems unlikely.
Discussion

An effect of the eluted components of ACSs (camphorquinone excepted) on the immunocompetent cells of the pulp, such as the T-cells, may be expected (117). None of the cited pulp-capping studies mentions sensitisation or allergic reactions. Epidermal contact with uncured composites and accessories may sensitise the individual and result in allergic skin reactions (118). Contact of ACSs with the oral mucosa may evoke delayed-type hypersensitivity immunologic (allergic) reactions in sensitised patients. Only a few cases have been reported (119). The lichenoid reactions of the mucosa in topographical contact with composite restorations (120, 121) represent a special situation where the immunological background is still uncertain. On the other hand, it is also conceivable that ACSs in contact with the oral mucosa could induce tolerance rather than sensitisation, just like metals may do in the oral environment (122). Of the methacrylates especially the comonomer HEMA may induce allergy (123, 124). Considerable amounts of HEMA were present in aqueous extract from four of ve adhesives, in particular from Syntac Sc (Vivadent, Lichtenstein) and, although less, from Scotchbond MultiPurpose (71). Immediate-type allergic reactions are sometimes associated with transcutaneous contacts. In sensitised individuals, contact of the pulpal tissue with components of composite systems theoretically could evoke

In many instances the older Ca(OH)2 formulations do not provide a long-term protection against microleakage, because they dissolve within 12 years, and tunnel defects in the majority of the dentin bridges then allow (recurrent) pulp inammation. The solubility of newer Ca(OH)2 formulations, such as Ultrablend VLCA [plusA]), has been reduced, but it is unknown whether these products provide a permanent seal. Ca(OH)2 cappings may be covered with the cements themselves is not warranted because of paucity of experimental data. Pulp cappings ACSs are at the moment the only realistic alternative to Ca(OH)2- products. Different adhesives, different acids in varying concentrations, 35% phosphoric acid possibly excepted, and different composites have been used with success. However, microleakage of some ACSs is a threat to the pulp on the short-term. Of other brands, absence of microleakage on the long-term has not been proven. The components of the ACSs are found to be toxic in cell cultures, but it may be doubted that pulp capping with ACSs are in general too toxic to the pulp. Also the temperature rise during photocuring of the ACSs does not seem to be harmful to the pulp. No data are 247

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available on sensitisation and allergic reactions following the placement of the ACSs on the pulp, thus denite conclusions cannot be drawn on this issue. It should be stressed that to the most part, only intentionally exposed pulps of healthy teeth in animals have been studied. Caries profunda was, however, no obstacle to successful capping with Dycal (8), but this does not mean that a pulp affected by the carious process will survive the toxic attack (and/or temperature rise) of the direct contact with ACSs. In conclusion: at the moment direct capping of exposed, vital pulps with the adhesive resin-based composites seems promising. There are indications, from short-term experiments, that the ACSs give highly variable results. Due to microleakage capping with some ACSs (see notes Table 2) is inferior to capping with Ca(OH)2. Furthermore, it seems advisable to avoid the use of 35% phosphoric acid and Consepsis. Longer-term evaluations are needed to see whether the ACSs perform as well as, or better than, Ca(OH)2 in the long run. Altogether, it seems hardly justied to treat accidentally exposed vital pulps with the ACSs.
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